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[*] posted on 12-11-2014 at 01:29


Quote: Originally posted by Morkva  
Perhaps "a complete lack of mechanistic explanation" was written to bait me, because it's foolish, or at least premature. Referring to them plausibly as "SERM's" I take to suggest you don't know other drugs, which were not SERMs, verified that the target is indeed NPC1. (edit: in fact, there were other demonstrations of this!) For that matter, while I imagine getting approval to work with ebola is monumentally difficult, at least one group from memory has expanded (implicitly confirming) on another's finding in this regard, with isolated luminescent cells no less.

Baiting? It's factual. Cite the proposed mechanism of SERM drugs in Ebola prophylaxis if you feel otherwise. A pathway is not a mechanism of action.
"It is not known whether clomiphene and toremifene (or other CADs) interact directly with NPC1 or mediate their effects indirectly through NPC1."
http://stm.sciencemag.org/content/5/190/190ra79

"Collectively, the results in Figs. 5, ​,6,6, and ​and77 suggest that the CADs that block EBOV entry do so by perturbing an NPC1-dependent pathway without, however, disrupting the direct interaction between NPC1 and primed EBOV GP."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575416/
(From your own source... which I assume you read and ignored while inveighing against a hobby chemistry forum from your moral pulpit, high on ignorance.)

Gee, no validated mechanism of action. Please stop talking about what you don't know.
You must be trolling. You mentioned two SERM drugs with no mechanistic explanation for any unsubstantiated efficacy, and said "why has toremifene not been publicized?" I just explained why.... Murine model data with low data sets have been published, and while valuable, that is limited in use, obviously.

As for claiming I'm ignorant of drugs... I just gave you a better example for your ridiculous temper tantrum! TKM-Ebola, which was just advanced from pre-clinical non-human private testing.

Quote:
Prophylaxis may be the proper target of the NPC1 mediated drugs,

Prophylaxis is not a target. Targets are drug receptors, and NPC1 has not been shown to be a SERM receptor. You clearly have no idea what you're talking about, so stop.

I have spoken about ANDA filing and safety profiles on approved drugs for new label use... and they are not "as good as it gets." Safety profiles don't have anything to do with efficacy. Most drugs fail in late clinical trials, often after efficacy is demonstrated. This is due to efficacy.

You are obviously oblivious to how biomedical research is carried out.

"Although this characterization of anti-filovirus activity of clomiphene and toremifene shows the potential for their use to treat Ebola virus disease, additional evaluation of these drugs in the NHP infection model is required to fully validate their use in a clinical setting. Both drugs showed activity in the murine infection model; however, many drugs that are active in this model have not proved efficacious in the NHP model."
http://stm.sciencemag.org/content/5/190/190ra79
For your edification.

Everything I've said is spot on. If you don't want to integrate it into your knowledge-base, fine. Stop flaming and making terrible assumptions about things you clearly aren't as knowledgeable in as you would like to be. Thanks.

I would be much more polite if you hadn't been so insulting, or apologized. For you to insult us and then be impressed by "isolated luminescent cells no less" is ridiculous. Most drugs fail in clinical trials... you know, after cell line and animal model efficacy looks awesome. People are different, complex and fairly heterogeneous with SNPs and idiosyncratic reactions. Only someone not in any kind of biomed/pharm field would be calling for human trials based on murine models. These aren't even primates, as I pointed out to you previously!

[Edited on 12-11-2014 by Chemosynthesis]
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[*] posted on 12-11-2014 at 02:59


Quote: Originally posted by Morkva  
No, you cited a different paper. There are several. Our argument may be fueled by you being unaware of those consequent to that screening.

Check out "Multiple Cationic Amphiphiles inhibit..." uh, whatever it's called. One I linked to. And Anna Bruchez's dissertation. Those expand on the mechanism. Oh! And I believe another has in it's title "NPC1 is necessary for...". There isn't just that one paper dude!

I cited two papers. Your paper does indeed support my point, actually. I probably didn't distinguish well enough, but if you make the claim (known mechanism of action), you need to cite the papers with a quote, preferably. Giving me a partial title of another paper, or saying there is more than one paper floating out in the internet isn't really a rational argument. You need to substantiate your point.

I was addressing SERMs, two of which you mentioned, and may theoretically be repurposed by an ANDA approval. These have known pharmacokinetic profiles. If you want to discuss other experimental therapies without known "drug-like" characteristics, which may not be viable therapeutics in and of their own rights, I'm not interested in talking about laboratory tools. Scientists make efficacious compounds as mechanistic probes all the time that would never work in human beings. This is common in theses in particular, since students don't run clinical trials.

To your paper and the SERM topic.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575416/
PLoS One. 2013; 8(2): e56265.
Published online Feb 18, 2013. doi: 10.1371/journal.pone.0056265
Multiple Cationic Amphiphiles inhibit...

1. "The goal of this study was to identify additional small molecule EBOV entry inhibitors, and to probe their mechanisms of action. As a result, we identified six structurally related cationic amphiphiles that specifically block a late stage of EBOV entry. All of the inhibitors induced cholesterol accumulation in LE/Lys and those tested showed shifted dose-response curves in NPC1-overexpressing cells. However, none blocked the interaction of primed GP with NPC1. These results suggest that there are at least two ways of interfering with NPC1-dependent mechanisms that block EBOV entry into the cytoplasm, and that structurally-related cationic amphiphiles may prove clinically useful in combating EBOV infection."

2. "Collectively, the results in Figs. 5 and ​and66 support our proposal that the CADs that block EBOV entry do so through an NPC1-dependent pathway. They do not, however, alter cellular expression levels of NPC1 (Supplemental Fig. S2)."

3. "Collectively, the results in Figs. 5, ​,6,6, and ​and77 suggest that the CADs that block EBOV entry do so by perturbing an NPC1-dependent pathway without, however, disrupting the direct interaction between NPC1 and primed EBOV GP."

I don't mean to diminish the research in the slightest, but it's not a known mechanism yet. Data supports a general pathway, and is seeming to rule out specific drug targets/mechanisms of action, but one hasn't been supported yet. Signaling pathways are huge, non-linear and often recursive.

The paper you cited also used glioma cells. Monoclonal cells for one single organ are not particularly valuable in determining patient drug efficacy, which I will explain in a moment. They have their uses, but they are the first line of investigation for research. You use them to get grants and expensive animal models.
http://www.lifetechnologies.com/us/en/home/technical-resourc...

Cell line data is used prior to animal data because it is not as useful as animal data in many ways. Cells lines are essentially monoclonal, in this case brain cancer, derived from one human being. They have severe limitations. Most organs are not the brain, are not grown in culture plates, and most brains don't have cancer. The longer you grow the cells, noted by a passage number, the weirder they behave. You start getting epigenetic quirks, chromosomal mutations, etc. because they are subtly being selected for what grows in a lab and not a person.
Additionally, everyone has unique DNA, and SNP mutations can cause interesting effects, such as Asians' stereotypical reactions to alcohol.

Quote: Originally posted by Morkva  


As for efficacy versus blah blah, if the SERMs habitually made supernumary ears sprout, or eyes to shrivel, organs fail etc. you'd still hear about it because of the approval process, and may not be approved even for breast cancer! Are you arguing that if something seems to be reasonably effective in what was a tolerable dose in the healthy, it may yet be toxic to the afflicted?

Okay, I am happy to define pharmacological terms for you if you like. I see where the misunderstanding may be stemming from. I am not trying to beat a dead horse, but if you don't know the difference between efficacy and toxicity, please apologize for insulting everyone in this thread, myself included.

Efficacy is the ability of a drug to bring about an intended therapeutic effect. In this case, inhibiting Ebola in a large population of people. A drug with a known safety profile may be safe by itself, but it may not actually treat a new disease.

It may also interact with medication that would, and so giving it out to people without any clinical human data suggesting efficacy is expensive, time consuming, and possibly even harmful in some cases. Even if it acts as a placebo, these resources could have been used trying to give palliative care or test other medications. Once you start trying to combine medications, you no longer have valid cohorts for determining what medication is helpful vs. what is not.

Keep in mind that most of the cases of Ebola are in Africa. The Western world can't just subject foreign citizens to experimental treatments, so bureaucracy is at play there. All U.S. patients receive one experimental drug for Ebola (ZMapp was one). Germany gave a patient FX06. These are just anecdotal cases, though. It's obviously unethical to just let someone get placebo for Ebola, but there should be enough WHO and CDC data from African hospitals to compare to.

The lack of data supporting SERM efficacy in people doesn't indicate it's of no efficacy in treating Ebola, no. I certainly don't mean to give that impression. However, giving people medications that act in ways we don't understand is hugely frowned upon by the FDA. I've seen drugs that obliterate all kinds of cancer cell lines and leave healthy cells alone... but that's not good enough to use in people yet. Evidence based medicine uses the scientific principles of substantiating efficacy and safety before advocating a drug.
Quote: Originally posted by Morkva  
Let me ask you: Infected with ebola, and with no medical attention, you're facing what looks like 7/10 chance of death (from what I understand was the situation for many).

Informed as you are right now, would you take toremifene?

Would you disdain it because it only worked in mice, and a small sample, it's mechanism is somewhat uncertain, and the side effects may unpredictably interact with the condition itself (as I understand your criticism to be)?

In what regard would you hold the one who refused you this choice to your face?

That's what "good enough for me" boils down too.

My opinion is irrelevant, as I don't consider myself educated enough on the specific treatment statistics to make a truly informed opinion, but if you really want my general opinion, something with demonstrated efficacy, or a hypothetical mechanism of action in actual human patients is always a more logical choice than an unknown. My personal preference may well hinge on what the Ebola specialist infectious disease physician and the CDC recommends, be it ZMAPP, FX06, plasma/antibodies, etc.
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[*] posted on 12-11-2014 at 03:37


Quote: Originally posted by Morkva  

But I never did consider giving out multiple unknown drugs that might interact with each other. For whatever that's worth. Seems unwise.

I'll make this brief because I'm likely to be unable to respond for several hours, but the combinatorial therapies are sometimes designed to function in conjunction with one another from inception. Example immediately below.
http://aac.asm.org/content/58/11/6639

Next quotes from http://emedicine.medscape.com/article/216288-treatment

Additionally, given that
"Currently, no specific therapy is available that has demonstrated efficacy in the treatment of Ebola hemorrhagic fever." there are some ethical considerations for clinicians whereby treatment with a promising adjunct, as long as you know the mechanisms of action and don't have data implying deleterious interaction, may be considered the highest quality of care. There are anecdotal examples and additional preclinical candidates cited in there.

It's unfortunate that in order to attain high fidelity data on efficacy, scientific controls sometimes limit what care can be given in order to compare new treatment outcomes with established ones. It's similar to how, in surgery, you can either have the latest technological advancement, or the most experienced surgeon. The first precludes the second. Obviously it gets awkward when there is no established treatment, like Ebola.
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[*] posted on 12-11-2014 at 08:07


In other news there are now no known active Ebola cases in the US.
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[*] posted on 12-11-2014 at 08:55


It is good there are no active cases in the U.S. however the risk of new cases increases absent travel restrictions and quarantine holds on travellers from the outbreak areas in Africa because the number of active cases being reported in Africa is increasing and is over a hundred new cases per day. The number of new cases reported in Africa is still slowly increasing and accellerating so that is indication the epidemic in Africa is growing and not subsiding. Passing time is not providing evidence the outbreak is burning itself out but on the contrary is continuing unchecked and is growing in seriousness. The problem with orphaned children of parents who died from ebola is a concern since many of those children orphaned in increasing numbers are probably infected but are not being monitored and are roaming about. The growing number of orphans, many of whom are themselves infected presents an increasing problem which challenges efforts to bring the outbreak under control. That terrible dilemma is a problem in Africa which bears consideration as one aspect of the good reasons for safeguards that would interfere with the spread of the outbreak and would keep the epidemic contained in Africa.

http://www.dailymail.co.uk/news/article-2829673/EXCLUSIVE-on...

The costs of the international effort to stop the outbreak based upon expenditures to the end of the past month is about a quarter million dollars per infected person in Africa and the epidemic is still increasing despite all efforts. The costs of countermeasures for cases not contained in Africa is multiplied greatly for other environments in more developed countries. So I would reiterate that the health care costs associated with this disease are catastrophic costs, even for the cases contained in Africa, and the costs would simply be unbearable in countries elsewhere if the epidemic spreads beyond Africa. So as a practical matter of the business REALITY all measures within reason should be taken to keep the epidemic confined to Africa, since the world simply can't afford the expense in either human terms or in monetary costs to allow that epidemic to spread beyond Africa. The world can't afford the luxury of unrestricted travel from epidemic areas when the potential costs for that reckless policy are not something that any country can later pay.
Unrestricted travel is like giving the ebola virus a blank check and allowing it to fill in the blank which becomes the bill that no nation can pay. The world lacks the wherewithal to cover its bet if it loses a reckless bet in a gamble with ebola.

[Edited on 12-11-2014 by Rosco Bodine]
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[*] posted on 12-11-2014 at 11:44
Expensive , I'll say


http://www.dailymail.co.uk/news/article-2830402/Inside-650-n...
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[*] posted on 12-11-2014 at 17:40


A headline about "avigan" set me off.

I can not help but be horrified that the "regulators" and doctors disagree that the two drugs which are already known to be tolerated by otherwise healthy humans, which were somewhat effective in mice, despite only a partially understood mechanism - but one which none the less seems plausible there is an analog of in humans, were not worth offering as an option, at the outset of this outbreak of a disease that kills upwards of one half of those infected (which is the main reason for my conclusion: debate about experimental treatments with comparable prospects could even be warranted by less-deadly diseases!) and which continues to threaten an international plague, never mind at this late stage where, as Rosco pointed out is still causing great expenditure, and is still causing deaths. In particular, they are simpler to prepare and to store than the still uncertain vaccines and antibodies, and more is known about their interaction with the human body than the other prospective antivirals.

And, my damnation was undeserved, but isn't it just a little incongruous that amateur scientists, whose nature is to independently satisfy their curiosity, look at literature, etc. should not have seized upon this, at least as tenaciously as to the many-paged debated about quarantines? Quarantines to prevent exposure to a disease with poorly explored treatment options, which can kill more than half infected depending on quality of care, and which has an incubation period up to 21 days in extreme cases. That gets debated on. "Incongruous."

Apology accepted?

[Edited on 13-11-2014 by Morkva]
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[*] posted on 12-11-2014 at 18:31


In the news, the duncan family has settled with the Presbyterian hospital in Dallas. Although the amount of the settlement was not released rumor is that the family settled for the maximum allowed by Texas law which is $250k per family member. Only the parents and children are eligible because he had not married his fiance. That would make the settlement $1.5 million. The hospital also agreed to set up a charity to fight Ebola.
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[*] posted on 12-11-2014 at 23:07


Quote: Originally posted by Morkva  
I can not help but be horrified that the "regulators" and doctors disagree that the two drugs which are already known to be tolerated by otherwise healthy humans, which were somewhat effective in mice, despite only a partially understood mechanism - but one which none the less seems plausible there is an analog of in humans, were not worth offering as an option, at the outset of this outbreak of a disease that kills upwards of one half of those infected (which is the main reason for my conclusion: debate about experimental treatments with comparable prospects could even be warranted by less-deadly diseases!) and which continues to threaten an international plague, never mind at this late stage where, as Rosco pointed out is still causing great expenditure, and is still causing deaths. In particular, they are simpler to prepare and to store than the still uncertain vaccines and antibodies, and more is known about their interaction with the human body than the other prospective antivirals.

What you are basically discussing is compassionate use/expanded access of experimental medications for terminal illnesses. In the U.S., the FDA regulates these with cost-benefit analyses. I have absolutely no idea how they work in African countries, but the FDA has no legal authority there, and so foreign laws are the business of foreign governments. I am assuming you want Western physicians to treat Africans, questions of off-label use legality arise. Do you have animosity towards U.S. and European physicians/regulators? If so, why? They have little authority to do anything to foreign citizens, and have to honor foreign law. It seems to me your anger should be directed more at African clinics, which are certainly not as capable of biotech/pharma research.

Again, this becomes an issue of potential efficacy over toxicity. TKM-Ebola is further in development, and was on hold to analyze data. The FDA changed that to a partial hold in order to speed up progress. Non-human primate efficacy data is more applicable to patients, and so that is arguably a better use of limited resources.

Additionally, clinicians in general and physicians in particular simply do not have enough time to read up on the latest scientific advances, nor are most of them qualified to do so in a critical manner. Clinicians are usually not scientists, and vice versa. Clinicians' rounds and patient care take up too much time to be deeply involved in analyzing science they are usually not specialized or participating in.

http://www.kevinmd.com/blog/2009/12/doctors-stay-date-curren...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1495716/

Ultimately, healthcare being a service, the extreme example is that if a physician were uncomfortable providing a specific treatment for any reason, it would be of questionable ethics to try and compel them to provide it against their volition. I knew a pediatrician who said they told parents who did not vaccinate children to use other doctors simply because they were not comfortable treating mumps or measles.

Quote:
And, my damnation was undeserved, but isn't it just a little incongruous that amateur scientists, whose nature is to independently satisfy their curiosity, look at literature, etc. should not have seized upon this, at least as tenaciously as to the many-paged debated about quarantines? Quarantines to prevent exposure to a disease with poorly explored treatment options, which can kill more than half infected depending on quality of care, and which has an incubation period up to 21 days in extreme cases. That gets debated on.

Apology accepted?

Yes, thank you. Hopefully I didn't come across as too rude.

SERM drugs were mentioned briefly: https://www.sciencemadness.org/whisper/viewthread.php?tid=38...
I'm not sure what else you want anyone here to say about them. I don't know how valid a glioma cell line is for Ebola models. The amount of reading to determine a "good" cell line (highly debatable) can be very prohibitive. I've seen contemptuous disagreement over receptor presence vs. functioning in monoclonal lines before. No one knew if having a non-functional receptor biased results vs. not having one at all, and the consensus was not to open that can of worms... change lines to one without a receptor and hope no one asks about the reason from switching given preceding data, assuming it's just a positive control to rule out experimental artifact.

I don't think that it's incongruous for an amateur science forum to not discuss SERM drugs in detail due to the impossibility in applying the subject to amateur science or experimentation. I (probably annoyingly) said several times in this thread the epidemiology is beyond amateur science and experimentalism as well.

As an example, here is part of a PM I had about SERM drugs which probably applies to this discussion.
"I understand your viewpoint on the disease being so disruptive that not treating people seems overly cautious. I don't know enough about the modified virus, and am not familiar enough with the Ebola genome to go into the GenBank sequences and compare to see how valid I expect those to be within a same-species test. Without very detailed mechanistic descriptions of pharmacological action, correlative studies can only be taken as suggestive of merit due to the huge discrepancies in human patients. Even with real human data in the thousands of patients, I've seen very large spreads of target expression which may it easy to accidentally confirm a bias of efficacy through poor statistical sampling."
(discussing http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955358/)
Again, even if mice are taken to be a valid model, when you order mice from the Trans-NIH Mouse Initiatives, you order very inbred strains. The paper did use the standard mouse model, from what I have seen in labs (not an animal expert), the C57BL/6... but the inbred genetics don't give us a very valid extrapolatory basis for diverse human patients.
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[*] posted on 13-11-2014 at 06:10


Breaking news: Liberia is lifting the state of emergency and allowing advanced trials of antivirals that have not passed preclinical or clinical trials, in addition to immunological transfusion therapy which has only had anecdotal data.
Ebola transmission still exponential and we have more than a month until we see if the CDC estimates for death tolls (1.5 million) were correct projections. Interestingly, reported death rates seem to be tapering off while exponential transmission still threatens the worst stats to come.

http://www.dailymail.co.uk/wires/ap/article-2832754/Medical-...

ebolastats.com
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[*] posted on 13-11-2014 at 18:05


The 1.5 million figure was with no outside intervention.
The key question is the effectiveness of the help.
The Liberia epidemic seems to have slowed for unknown
reasons while the infection rate in Sierra Leone has exploded.
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[*] posted on 14-11-2014 at 03:41


Quote: Originally posted by macckone  
The 1.5 million figure was with no outside intervention.
The key question is the effectiveness of the help.
The Liberia epidemic seems to have slowed for unknown
reasons while the infection rate in Sierra Leone has exploded.

"If trends continue without additional interventions, the model estimates that Liberia and Sierra Leone will have approximately 8,000 total Ebola cases (21,000 total cases when corrected for underreporting) by September 30, 2014 (Figure 1)."
http://www.cdc.gov/vhf/ebola/outbreaks/2014-west-africa/qa-m...
September/October estimates were spot on. Ebolastats.com

Granted "The U.S. government and international organizations recently announced commitments to support these measures. As these measures are rapidly implemented and sustained, the higher projections presented in this report become very unlikely."

That said, the report does claim that with rapid intervention, the highest estimates are unlikely. Speed is a big factor to keep in mind in addition to effectiveness. "MSF has sharply criticized the international response to the outbreak as slow and inadequate. Its international president, Joanne Liu, delivered that message to the United Nations in September."
http://www.voanews.com/content/ebola-crisis-puts-doctors-wit...

One the flipside, Doctors Without Borders is being criticized for not asking for vaccines earlier.
http://www.utahpeoplespost.com/2014/11/msf-accused-of-wastin...

"We wasted time before speaking about a vaccine and treatments... It's very hard to imagine controlling this epidemic now without a vaccine." http://uk.reuters.com/article/2014/11/14/us-health-ebola-msf...

http://www.doctorswithoutborders.org/news-stories/voice-fiel...



MSF has sharply criticized the international response to the outbreak as slow and inadequate. Its international president, Joanne Liu, delivered that message to the United Nations in September."
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[*] posted on 17-11-2014 at 06:14


sLiterally none of that poster's posts have been on topic, truthful, or otherwise valid.

In other news, we now have the first Ebola fatality in the state,unfortunately. He was initially symptomatic but tested negative for Ebola. http://www.foxnews.com/health/2014/11/17/surgeon-who-contrac...

edit state. not U.S. after Duncan.

[Edited on 17-11-2014 by Chemosynthesis]
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[*] posted on 17-11-2014 at 08:51


Second, and again treatment was delayed until he had been symptomtic for quite some time.
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[*] posted on 17-11-2014 at 08:56


Quote: Originally posted by Chemosynthesis  
Literally none of that poster's posts have been on topic, truthful, or otherwise valid.

In other news, we now have the first Ebola fatality in the U.S., unfortunately. He was initially symptomatic but tested negative for Ebola. http://www.foxnews.com/health/2014/11/17/surgeon-who-contrac...

This is the second Ebola fatality in the US.
One interesting question is what caused the negative test
given that he was symptomatic. One possibility is testing in
Sierra Leone is substandard. Another possibility is that he had
a co-infection causing fever, vomiting and other symptoms.
Given the number of infections that can cause similar early
symptoms that are rampant in that part of the world it
is conceivable that his initial symptoms were something
as common as food poisoning. And that having two
infections could lead to a much worse outcome.
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[*] posted on 17-11-2014 at 08:58


Given that half of the patients receiving ZMAPP have died,
I have to question its effectiveness. However given the
small sample size, it may not mean anything.
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[*] posted on 17-11-2014 at 10:12


Mali had a cluster recently as well. http://abcnews.go.com/Health/wireStory/mali-high-alert-ebola...
Quote: Originally posted by Spock  
Second, and again treatment was delayed until he had been symptomtic for quite some time.
Yep, thanks both. I mistyped. I meant state since Duncan was TX. Wasn't typing what I was thinking since I was on the way out the door and didn't even get my coffee. Probably also subconsciously biased due to his employ and residency (first U.S. resident and a hospital employee), unfortunately. The location is significant because two other patients were treated there. Bear in mind ZMAPP is not the only drug used, so patients aren't even in the same cohort due to combinatorial therapy; Richard Sacra received TKM-Ebola in the hospital and Ashoka Mukpo, Brincidofovir. Not even racial disparity has been taken info account due to low n.

The most interesting point about the delay was the false negative (assuming no alternative initial infection, which is possible if replication rates don't imply otherwise), which makes me wonder what type of test was used. The equipment in Dallas was approved solely for research, not therapeutic diagnostics, in Duncan's case... but it is worth noting that I have posted mutation analysis where diagnostic proteins have seen high mutation rates. It would be nice if more information were available on the types of tests provided on location. Being symptomatic, and with Ebola's very high virulence, it's assumed Salia was contagious with a titer below the limit of quantitation of the test used. This doesn't seem unusual given the quote: http://www.washingtonpost.com/world/a-doctors-mistaken-ebola...

Even false negatives with PCR are noted in the literature: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC139694/

With a false negative, bloody diarrhea or vomit could easily be mis identified as a GI bleed or pigmentation from bismuth subsalicylate (try dictating that one).

[Edited on 17-11-2014 by Chemosynthesis]
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[*] posted on 19-11-2014 at 10:51


Man cured of ebola is quarantined in India because the virus was detected in his seamen. The virus remains in seamen for > 90 days. Also there are 45,000 Indians living in west Africa.

http://www.bbc.com/news/world-asia-india-30105290
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aga
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[*] posted on 19-11-2014 at 12:36


Many Indian descendants in south east Africa too.

I doubt that they have super-ebola harbouring sperm though.

Fact is that touchy-feely, random-inserty is what gives Africa it's terrible problems with HIV and now Ebola.

The Claims of 'airbourne' are spurious.

It's transfer is via fluid exchange, amplified in Africa by many culture-reinforced mechanisms.




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[*] posted on 20-11-2014 at 16:16


Gotta love how infowars says the brooklyn woman who was on
ebola watch was bleeding from mouth and eyes when in reality
it was simply a heart attack. And testing was negative and she
was near the end of the 21 day period. This false information
is what is really hurting attacking the problem with science.
To date my understanding is ten people have been treated
for ebola in the US and only two have died.

The ones I am aware of are: Brantley and Whitbol, two missionaries
that were flown in on medical flights and treated at Emory, Sacra (not
a lot of information other than treatment in Nebraska), another
unnamed person at Emory, Mukpo (journalist, treated in Nebraska),
Duncan (who died) and his two nurses, Vinson and Pham (all in Dallas),
Spencer (the doctor from NY), And the latest Salia who died.
http://abcnews.go.com/Health/ebola-america-timeline/story?id...

Does anyone know of any other actual ebola cases?
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[*] posted on 21-11-2014 at 06:37


That's it as far as I know for confirmed U.S. cases.
I was surprised this one didn't get more conspiracy attention:
http://online.wsj.com/articles/ebola-alert-sparks-false-alar...
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[*] posted on 21-11-2014 at 10:03


That is why the CDC has asked the news media to stop reporting
unconfirmed cases. Too many people get ill after traveling to
foreign countries. There have been a lot of people returning
from Africa with various illnesses, usually in the food poisoning
or water borne illness categories. Americans simply don't have
resistance to many of the pathogens that are endemic in
other countries that natives are immune to.
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[*] posted on 21-11-2014 at 11:51


The biggest problem with Conspiracy theories is that they seem to want to fly off into the realms of Fantasy, when there is absolutely no need.

In every single case there is a Powerful Interested party which perpetrates whatever action for their own Gain.

E.g. Twin Towers video inconsistent. Plane impact defies physics.

Yes. Correct. The Lie is kinda proven. So what?
The populace swallowed the 'terrorist' story, and ignored the cruise/hellfire strike on the pentagon.
Job done.
Neither Truth nor the Facts have anything to do with it.
Aliens ? Certainly not.

As a direct consequence, war in Afghanistan so an oil/gas pipeline can be built.

The idea that any US government would Not kill lots of it's own civilians in order to further it's own aims is ridiculous. Sure as s**t have had a lot of practice killing civilians.

Gotta say that they really pulled off a Big one with that gig though, despite many silly mistakes.

[Edited on 21-11-2014 by aga]




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[*] posted on 21-11-2014 at 11:54


Forgot to mention: I'm going to Africa next year !



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[*] posted on 21-12-2014 at 15:16


http://www.infowars.com/fox-investigation-cdc-may-be-hiding-...

Interesting.




"Science is the belief in the ignorance of the experts" Richard Feynman
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